Mesenchymal-epithelial transition (MET) as a mechanism for metastatic colonisation in breast cancer

Cancer Metastasis Rev. 2012 Dec;31(3-4):469-78. doi: 10.1007/s10555-012-9377-5.


As yet, there is no cure for metastatic breast cancer. Historically, considerable research effort has been concentrated on understanding the processes of metastasis, how a primary tumour locally invades and systemically disseminates using the phenotypic switching mechanism of epithelial to mesenchymal transition (EMT); however, much less is understood about how metastases are then formed. Breast cancer metastases often look (and may even function) as 'normal' breast tissue, a bizarre observation against the backdrop of the organ structure of the lung, liver, bone or brain. Mesenchymal to epithelial transition (MET), the opposite of EMT, has been proposed as a mechanism for establishment of the metastatic neoplasm, leading to questions such as: Can MET be clearly demonstrated in vivo? What factors cause this phenotypic switch within the cancer cell? Are these signals/factors derived from the metastatic site (soil) or expressed by the cancer cells themselves (seed)? How do the cancer cells then grow into a detectable secondary tumour and further disseminate? And finally--Can we design and develop therapies that may combat this dissemination switch? This review aims to address these important questions by evaluating long-standing paradigms and novel emerging concepts in the field of epithelial mesencyhmal plasticity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Breast Neoplasms / pathology*
  • Cadherins / analysis
  • Cell Proliferation
  • Epithelial-Mesenchymal Transition*
  • Female
  • Humans
  • Neoplasm Invasiveness
  • Neoplasm Metastasis / pathology*
  • Tumor Microenvironment


  • Cadherins